Osteoporosis and related factors in older females with skeletal pain or numbness: A retrospective study in East China

Yong-sheng, Zhao; Liu, Yuxin; Zheng, Yanping

doi:10.1177/0300060513483414

Cited by 3 publications

(6 citation statements)

References 24 publications

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“…Osteoporosis is one of the most prevalent degenerative diseases affecting elderly people [1,2] and is characterized by low bone mass, altered bone microarchitecture and increased risk of fracture [1,2]. Multiple factors have been implicated in the development of osteoporosis, including gender, age, body weight, sustained glucocorticoid therapy and endocrinological disorders [1,3].…”

Section: Introductionmentioning

confidence: 99%

Blockade of Drp1 rescues oxidative stress-induced osteoblast dysfunction

Gan

Huang

et al. 2015

Biochemical and Biophysical Research Communications

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Osteoblast dysfunction, induced by oxidative stress, plays a critical role in the pathophysiology of osteoporosis. However, the underlying mechanisms remain unclarified. Imbalance of mitochondrial dynamics has been closely linked to oxidative stress. Here, we reveal an unexplored role of dynamic related protein 1(Drp1), the major regulator in mitochondrial fission, in the oxidative stress-induced osteoblast injury model. We demonstrate that levels of phosphorylation and expression of Drp1 significantly increased under oxidative stress. Blockade of Drp1, through pharmaceutical inhibitor or gene knockdown, significantly protected against H2O2-induced osteoblast dysfunction, as shown by increased cell viability, improved cellular alkaline phosphatase (ALP) activity and mineralization and restored mitochondrial function. The protective effects of blocking Drp1 in H2O2-induced osteoblast dysfunction were evidenced by increased mitochondrial function and suppressed production of reactive oxygen species (ROS). These findings provide new insights into the role of the Drp1-dependent mitochondrial pathway in the pathology of osteoporosis, indicating that the Drp1 pathway may be targetable for the development of new therapeutic approaches in the prevention and the treatment of osteoporosis.

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Section: Introductionmentioning

confidence: 99%

Blockade of Drp1 rescues oxidative stress-induced osteoblast dysfunction

Gan

Huang

et al. 2015

Biochemical and Biophysical Research Communications

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“…Osteoporosis is a skeletal disease characterised by an increased bone turnover with insufficient bone formation relative to bone resorption, leading to increased bone fragility and increased fracture risk (Graat-Verboom et al, 2009;Zhao et al, 2013). Multiple factors have been implicated to associate with osteoporosis, including gender, age, body weight, sustained glucocorticoid therapy and endocrinological disorders (Zhao et al, 2013;Abe et al, 2007;Compston, 1992).…”

Section: Introductionmentioning

confidence: 99%

“…Multiple factors have been implicated to associate with osteoporosis, including gender, age, body weight, sustained glucocorticoid therapy and endocrinological disorders (Zhao et al, 2013;Abe et al, 2007;Compston, 1992). Particularly, osteoporosis has been a major public health threat for the elderly, particularly for postmenopausal women, where it is called postmenopausal osteoporosis (Ozgocmen et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Grape seed proanthocyanidins inhibit H2O2-induced osteoblastic MC3T3-E1 cell apoptosis via ameliorating H2O2-induced mitochondrial dysfunction

et al. 2014

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-Oxidative stress represents a major cause of cellular damage and death in pathological conditions including osteoporosis, in which oxidative stress is associated with increased bone resorption and low bone mass. And grape seed proanthocyanidins are a group of polyphenolic bioflavonoids which are known to possess broad pharmacological activity and therapeutic potential, exerting a protective role against oxidant injury. The aim of our study was to investigate whether proanthocyanidins exert an anti-apoptosis effect in osteoblastic MC3T3-E1 cells, via their antioxidant activity. Firstly, we determined the anti-apoptosis effect of proanthocyanidins in osteoblastic MC3T3-E1 cells, which were subject to H 2 O 2 treatment, then we determined the association of the antioxidant activity exerted by proanthocyanidins with their anti-apoptosis effect. Results demonstrated that proanthocyanidins inhibit H 2 O 2 -promoted apoptosis in MC3T3-E1 cells, via ameliorating the viability of MC3T3-E1 cells post H 2 O 2 treatment and reducing the apoptotic cell numbers. And the proanthocyanidins treatment also ameliorates the H 2 O 2 -induced mitochondrial dysfunction via promoting the mitochondrial membrane potential (MMP) and respiratory chain complex IV, and reducing the mitochondrial free radical production, ROS and mitochondrial superoxide. Moreover, the proanthocyanidins inhibit H 2 O 2 -induced apoptosis signaling which is mediated by p53. This study implied a possible anti-osteoporosis effect of proanthocyanidins via their antioxidant and anti-apoptosis activity.

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“…Osteoporosis is a skeletal disease characterized by the loss of bone mass and degeneration of bone microstructure, which results in an increased risk of fracture (1,2). Various physiological or pathological factors, such as menopause, age, sustained glucocorticoid therapy and endocrine disorders, contribute to osteoporosis (2)(3)(4).…”

Section: Introductionmentioning

confidence: 99%

“…Various physiological or pathological factors, such as menopause, age, sustained glucocorticoid therapy and endocrine disorders, contribute to osteoporosis (2)(3)(4). Over half of women aged >50 years old will suffer from osteoporosis or osteoporotic fracture during their lifetime (5).…”

Section: Introductionmentioning

confidence: 99%

Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells

Ding

Zhao

Jiang

2016

Experimental and Therapeutic Medicine

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Abstract.Osteoporosis is a disease of the skeleton that is characterized by the loss of bone mass and degeneration of bone microstructure, resulting in an increased risk of fracture. Oxidative stress, which is known to promote oxidative damage to mitochondrial function and also cell apoptosis, has been recently indicated to be implicated in osteoporosis. However, there are few agents that counteract oxidative stress in osteoporosis. In the present study, the protective effects of allicin against the oxidative stress-induced mitochondrial dysfunction and apoptosis were investigated in murine osteoblast-like MC3T3-E1 cells. The results demonstrated that allicin counteracted the reduction of cell viability and induction of apoptosis caused by hydrogen peroxide (H 2 O 2 ) exposure. The inhibition of apoptosis by allicin was confirmed by the inhibition of H 2 O 2 -induced cytochrome c release and caspase-3 activation. Moreover, the inhibition of apoptosis by allicin was identified to be associated with the counteraction of H 2 O 2 -induced mitochondrial dysfunction. In addition, allicin was demonstrated to be able to significantly ameliorate the repressed phosphoinositide 3-kinase (PI3K)/AKT and cyclic adenosine monophosphate response element-binding protein (CREB)/extracellular-signal-regulated kinase (ERK) signaling pathways by H 2 O 2 , which may also be associated with the anti-oxidative stress effects of allicin. In conclusion, allicin protects osteoblasts from H 2 O 2 -induced oxidative stress and apoptosis in MC3T3-E1 cells by improving mitochondrial function and the activation of PI3K/AKT and CREB/ERK signaling. The present study implies a promising role of allicin in oxidative stress-associated osteoporosis.

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Osteoporosis and related factors in older females with skeletal pain or numbness: A retrospective study in East China

Abstract: The present study revealed a relationship between epidemiological distribution of osteoporosis and associated factors in adult females suffering from pain or numbness, in East China.

Cited by 3 publications

References 24 publications

Blockade of Drp1 rescues oxidative stress-induced osteoblast dysfunction

Blockade of Drp1 rescues oxidative stress-induced osteoblast dysfunction

Grape seed proanthocyanidins inhibit H<sub>2</sub>O<sub>2</sub>-induced osteoblastic MC3T3-E1 cell apoptosis via ameliorating H<sub>2</sub>O<sub>2</sub>-induced mitochondrial dysfunction

Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells

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